Comparison of the response to angiotensin II of isolated dog coronary and mesenteric arteries of proximal and distal portions.

Helically cut strips of dog coronary and mesenteric arteries of proximal and distal portions contracted in response to angiotensin (ANG) II in a dose-dependent fashion. The contractions were greater in the distal portions than in the proximal portions. Mesenteric arteries responded to the peptide with a greater contraction than coronary arteries. The peptide-induced contraction was suppressed by treatment with saralasin and was potentiated by indomethacin; magnitudes of the potentiation were similar in coronary and mesenteric arteries and in proximal and distal portions. Concentrations of TRK-100, a stable analog of PGI2, equipotent to those of PGI2 released by ANG II, estimated from dose-response curves for TRK-100 and enhancement by indomethacin of ANG II-induced contractions, did not differ in proximal and distal portions. It appears that differences in the contractile response to ANG II depend on heterogeneity in ANG II receptors responsible for the arterial contraction, but not on differences in the PGI2 generation via ANG II receptor activation.